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Westley H. Reeves - One of the best experts on this subject based on the ideXlab platform.

  • interleukin 6 dependence of anti dna Antibody production evidence for two pathways of autoAntibody formation in pristane induced lupus
    Journal of Experimental Medicine, 1998
    Co-Authors: Hanno B. Richards, Melody Shaw, Claude Libert, Valeria Poli, Minoru Satoh, Westley H. Reeves
    Abstract:

    Pristane induces a lupus-like syndrome in nonautoimmune mice characterized by the development of glomerulonephritis and lupus-associated autoantibodies. This is accompanied by overproduction of interleukin (IL)-6, a cytokine linked with autoimmune phenomena. The goal of this study was to evaluate the role of IL-6 in autoAntibody production in pristane-induced lupus. BALB/cAn IL-6–deficient (−/−) and –intact (+/+) mice were treated with pristane or phosphate-buffered saline, and autoAntibody production was evaluated. Pristane induced high levels of immunoglobulin (Ig)G anti-single-stranded DNA, –double-stranded (ds)DNA, and -chromatin antibodies in IL-6+/+, but not IL-6−/− mice by enzyme-linked immunosorbent assay. High titer IgG anti-dsDNA antibodies also were detected in sera from +/+, but not −/−, mice by Crithidia luciliae kinetoplast staining. The onset of IgG anti-dsDNA Antibody production in +/+ mice occurred >5 mo after pristane treatment, well after the onset of nephritis, suggesting that these antibodies are not directly responsible for inducing renal disease. In contrast to anti-DNA, the frequencies of anti-nRNP/Sm and anti-Su antibodies were similar in pristane-treated IL-6−/− and IL-6+/+ mice. However, levels were higher in the +/+ group. These results suggest that IgG anti-DNA and chromatin antibodies in pristane-treated mice are strictly IL-6 dependent, whereas induction of anti-nRNP/Sm and Su autoantibodies is IL-6 independent. The IL-6 dependence of anti-DNA, but not anti-nRNP/Sm, may have implications for understanding the patterns of autoAntibody production in lupus. Anti-DNA antibodies are produced transiently, mainly during periods of disease activity, whereas anti-nRNP/Sm Antibody levels are relatively insensitive to disease activity. This may reflect the differential IL-6 dependence of the two responses.

L U Yiyu - One of the best experts on this subject based on the ideXlab platform.

Hanno B. Richards - One of the best experts on this subject based on the ideXlab platform.

  • interleukin 6 dependence of anti dna Antibody production evidence for two pathways of autoAntibody formation in pristane induced lupus
    Journal of Experimental Medicine, 1998
    Co-Authors: Hanno B. Richards, Melody Shaw, Claude Libert, Valeria Poli, Minoru Satoh, Westley H. Reeves
    Abstract:

    Pristane induces a lupus-like syndrome in nonautoimmune mice characterized by the development of glomerulonephritis and lupus-associated autoantibodies. This is accompanied by overproduction of interleukin (IL)-6, a cytokine linked with autoimmune phenomena. The goal of this study was to evaluate the role of IL-6 in autoAntibody production in pristane-induced lupus. BALB/cAn IL-6–deficient (−/−) and –intact (+/+) mice were treated with pristane or phosphate-buffered saline, and autoAntibody production was evaluated. Pristane induced high levels of immunoglobulin (Ig)G anti-single-stranded DNA, –double-stranded (ds)DNA, and -chromatin antibodies in IL-6+/+, but not IL-6−/− mice by enzyme-linked immunosorbent assay. High titer IgG anti-dsDNA antibodies also were detected in sera from +/+, but not −/−, mice by Crithidia luciliae kinetoplast staining. The onset of IgG anti-dsDNA Antibody production in +/+ mice occurred >5 mo after pristane treatment, well after the onset of nephritis, suggesting that these antibodies are not directly responsible for inducing renal disease. In contrast to anti-DNA, the frequencies of anti-nRNP/Sm and anti-Su antibodies were similar in pristane-treated IL-6−/− and IL-6+/+ mice. However, levels were higher in the +/+ group. These results suggest that IgG anti-DNA and chromatin antibodies in pristane-treated mice are strictly IL-6 dependent, whereas induction of anti-nRNP/Sm and Su autoantibodies is IL-6 independent. The IL-6 dependence of anti-DNA, but not anti-nRNP/Sm, may have implications for understanding the patterns of autoAntibody production in lupus. Anti-DNA antibodies are produced transiently, mainly during periods of disease activity, whereas anti-nRNP/Sm Antibody levels are relatively insensitive to disease activity. This may reflect the differential IL-6 dependence of the two responses.

Minoru Satoh - One of the best experts on this subject based on the ideXlab platform.

  • interleukin 6 dependence of anti dna Antibody production evidence for two pathways of autoAntibody formation in pristane induced lupus
    Journal of Experimental Medicine, 1998
    Co-Authors: Hanno B. Richards, Melody Shaw, Claude Libert, Valeria Poli, Minoru Satoh, Westley H. Reeves
    Abstract:

    Pristane induces a lupus-like syndrome in nonautoimmune mice characterized by the development of glomerulonephritis and lupus-associated autoantibodies. This is accompanied by overproduction of interleukin (IL)-6, a cytokine linked with autoimmune phenomena. The goal of this study was to evaluate the role of IL-6 in autoAntibody production in pristane-induced lupus. BALB/cAn IL-6–deficient (−/−) and –intact (+/+) mice were treated with pristane or phosphate-buffered saline, and autoAntibody production was evaluated. Pristane induced high levels of immunoglobulin (Ig)G anti-single-stranded DNA, –double-stranded (ds)DNA, and -chromatin antibodies in IL-6+/+, but not IL-6−/− mice by enzyme-linked immunosorbent assay. High titer IgG anti-dsDNA antibodies also were detected in sera from +/+, but not −/−, mice by Crithidia luciliae kinetoplast staining. The onset of IgG anti-dsDNA Antibody production in +/+ mice occurred >5 mo after pristane treatment, well after the onset of nephritis, suggesting that these antibodies are not directly responsible for inducing renal disease. In contrast to anti-DNA, the frequencies of anti-nRNP/Sm and anti-Su antibodies were similar in pristane-treated IL-6−/− and IL-6+/+ mice. However, levels were higher in the +/+ group. These results suggest that IgG anti-DNA and chromatin antibodies in pristane-treated mice are strictly IL-6 dependent, whereas induction of anti-nRNP/Sm and Su autoantibodies is IL-6 independent. The IL-6 dependence of anti-DNA, but not anti-nRNP/Sm, may have implications for understanding the patterns of autoAntibody production in lupus. Anti-DNA antibodies are produced transiently, mainly during periods of disease activity, whereas anti-nRNP/Sm Antibody levels are relatively insensitive to disease activity. This may reflect the differential IL-6 dependence of the two responses.

  • nonprecipitating igg or igm anti Sm Antibody clinical significance and changes in immunoglobulin class
    The Journal of Rheumatology, 1993
    Co-Authors: K Tsuzaka, Minoru Satoh, Takashi Ogasawara, Takeshi Tojo, Tsuneyo Mimori, Mitsuo Homma
    Abstract:

    OBJECTIVE To estimate the clinical significance of IgG or IgM nonprecipitating anti-Sm antibodies and their immunoglobulin (Ig) class switch. METHODS Ninety-one sera which were positive for anti-nRNP antibodies by double immunodiffusion (DID) were obtained from patients with various rheumatic diseases. Anti-Sm Antibody was detected by RNA-immunoprecipitation (RNA-IP). IgG or IgM anti-Sm Ig class was measured by enzyme linked immunosorbent assay using affinity purified D polypeptide from HeLa cells. One hundred sixteen clinical manifestations were compared among these groups of patients. RESULTS By RNA-IP and DID, 91 were divided into 43 with nonprecipitating anti-Sm which were not detected by DID but by RNA-IP, 17 no anti-Sm, and 31 precipitating anti-Sm sera. In 43 patients with nonprecipitating anti-Sm, renal involvement was more common than in no anti-Sm patients. Besides, systemic lupus erythematosus (SLE)-type manifestations were less common than in precipitating anti-Sm patients. In these 43 patients, IgM anti-Sm class was common (13/43). Decrease in the ratio of IgM to IgG anti-Sm Antibody was observed in proportion to the years of observation in these patients. IgM anti-Sm predominated in these patients with mixed connective tissue disease (MCTD)-type manifestations while IgG anti-Sm did in those with SLE-type features. CONCLUSIONS Patients with nonprecipitating anti-Sm who have IgM anti-Sm at early stages of disease are more likely to have MCTD-type manifestations and later may shift to SLE-type features. These may reflect the anti-Sm Ig class switches from IgM to IgG.

John A Hardin - One of the best experts on this subject based on the ideXlab platform.

  • autoantigenic epitopes of the b and d polypeptides of the u1 snrnp analysis of domains recognized by the y12 monoclonal anti Sm Antibody and by patient sera
    Journal of Immunology, 1993
    Co-Authors: Michito Hirakata, J Craft, John A Hardin
    Abstract:

    Anti-Sm antibodies, a specific marker for SLE, are directed against the B'/B and D polypeptides of Sm Small nuclear ribonucleoproteins. The Y12 monoclonal anti-Sm Antibody (Y12 mAb), as well as many anti-Sm patient sera, recognize cross-reactive epitopes on the B'/B and D polypeptides. This immunoreactive site is of special interest since polypeptides B and D share little amino acid sequence homology. In the present study, we have sought to establish the autoantigenic domain of polypeptides B and D that accounts for this epitope. We tested the ability of the Y12 mAb and anti-Sm sera to immunoprecipitate truncated forms of polypeptides B and D translated in vitro from mRNA bearing 5' and 3' end deletions. Most anti-Sm sera bound epitopes at the carboxyl-terminus of polypeptide B, however, autoantigenic epitopes were also found at the amino-terminus (amino acids 1 to 83 and 104 to 115). Surprisingly, the Y12 mAb recognized nonoverlapping amino-terminal and carboxyl-terminal halves of polypeptide B. One putative Y12 mAb binding site (amino acids 104 to 115) indicated by carboxyl-terminal deletion studies was confirmed through recognition of a corresponding synthetic peptide. Deletion studies with polypeptide D demonstrated a major autoantigenic domain on the carboxyl-terminus (amino acids 85 to 119) that was necessary for recognition by the Y12 mAb and by 7/14 patient sera. These results indicate that a cross-reactive epitope on B'/B and D, as defined by the Y12 mAb, resides on at least two different domains of polypeptide B and localizes to the carboxyl-terminus of polypeptide D. From the shared homology of truncated forms of B and D polypeptides recognizable with the Y12 mAb, we suspect that some form of GRG motif is involved in developing the Y12 mAb epitope that may involve other residues and be largely conformational in nature.